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The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [ChIP-Seq]

ABSTRACT: WDR5 is an important co-factor for N-Myc-regulated transcriptional activation and tumorigenesis Using ChIP-Seq, We profiled key epigenetic marks H3K4 trimethylation in BE(2)-C neuroblastoma cells transfected with control siRNA or WDR5 siRNA-1 at N-Myc target gene promoters The results showed knockdown WDR5 significantly reduced H3K4me3 at 93.2% of N-Myc binding promoters, but only at 53.5% of N-Myc non-binding promoters.

ORGANISM(S): Homo sapiens

PROVIDER: GSE70098 | GEO | 2015/12/31

SECONDARY ACCESSION(S): PRJNA287646

REPOSITORIES: GEO

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The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [ChIP-Seq]

Project description:WDR5 is an important co-factor for N-Myc-regulated transcriptional activation and tumorigenesis Using ChIP-Seq, We profiled key epigenetic marks H3K4 trimethylation in BE(2)-C neuroblastoma cells transfected with control siRNA or WDR5 siRNA-1 at N-Myc target gene promoters The results showed knockdown WDR5 significantly reduced H3K4me3 at 93.2% of N-Myc binding promoters, but only at 53.5% of N-Myc non-binding promoters. Identification of Histone H3K4 trimethylation and N-Myc binding sites in BE(2)-C cells transfected with control siRNA or WDR5 siRNA-1.

2015-12-31 | E-GEOD-70098 | biostudies-arrayexpress

The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [gene expression]

Project description:WDR5 is an important co-factor for N-Myc-regulated transcriptional activation and tumorigenesis We analysed whether WDR5 siRNAs modulate gene expression Neuroblastoma BE(2)-C cells were treated with control siRNA, WDR5 siRNA-1, and WDR5 siRNA-2 for 40 hours, and subjected to differential gene expression studies with Affymetrix microarrays.

2015-12-31 | E-GEOD-69861 | biostudies-arrayexpress

A Role for WDR5 in Integrating Threonine 11 Phosphorylation to Lysine 4 Methylationon Histone H3 and in Prostate Cancer

Project description:Upon androgen stimulation, PKN1-mediated histone H3 threonine 11 phosphorylation (H3T11P) promotes AR target genes activation. However, the underlying mechanism is not completely understood. Here, we show that WDR5, a subunit of the SET1/MLL complex, interacts with H3T11P and this interaction facilitates the recruitment of the SET1/MLL complex and subsequent H3K4 trimethylation (H3K4me3). Using ChIP-seq, we find that androgen stimulation results in a six-fold increase in the number of H3T11P-marked regions and induces WDR5 colocalization to one third of H3T11P-enriched promoters, thus establishing a genome-wide relationship between H3T11P and recruitment of WDR5. Accordingly, PKN1 knock-down or chemical inhibition severely blocks WDR5 association and H3K4me3 on AR target genes. Finally, WDR5 is critical in prostate cancer cell proliferation, and is hyperexpressed in human prostate cancers. Together, these results identify WDR5 as a critical epigenomic integrator of histone phosphorylation and methylation and a major driver of androgen-dependent prostate cancer cell proliferation. Identification of Histone 3 threonine 11 phosphorylation (H3T11P) marks and WDR5 binding sites in LNCaP cells treated with R1881 ligand (androgen) or solvent control.

2014-07-01 | E-GEOD-55279 | biostudies-arrayexpress

A Role for WDR5 in Integrating Threonine 11 Phosphorylation to Lysine 4 Methylationon Histone H3 and in Prostate Cancer

2014-07-01 | GSE55279 | GEO

The histone H3 lysine 4 presenter WDR5 induces N-Myc target gene transcription and promotes neuroblastoma [gene expression]

Project description:WDR5 is an important co-factor for N-Myc-regulated transcriptional activation and tumorigenesis We analysed whether WDR5 siRNAs modulate gene expression

2015-12-31 | GSE69861 | GEO

Proteomics analysis with the WDR5 PROTACs

Project description:Active gene transcription requires accessible chromatin. Post-translational modifications of histone proteins modulate accessibility to target genes, a process that is controlled by multiple chromatin modifying enzymes, remodelers and epigenetic reader proteins. Histone H3K4 methylation serves as hallmark of actively transcribed genes and is introduced by histone methyltransferases (HMTs). For proper function of HMT activity, several adaptor proteins are required. One of these proteins is the WD-repeat containing protein 5 (WDR5) that acts as scaffolding component in HMT complexes and that has been associated with controlling transcription factors including MYC and long non-coding RNAs. The wide influence of dysfunctional HMTs complexes and the typically upregulated MYC levels in diverse tumor types has made WDR5 an attractive cancer drug target. Indeed, protein-protein interface inhibitors for two protein interaction interfaces on WDR5 have been developed. While such compounds only inhibit a subset of WDR5 interactions, chemically induced proteasomal degradation of WDR5 might be an elegant way to target all oncogenic function. In this study, we present the design, synthesis and evaluation of two diverse WDR5 degrader series based on two WIN site binding scaffolds. We show that linker nature and length are essential for successful degradation and strongly influences the degradation rate. In the presented datasets, we determined the intracellular degradation specificity of the WDR5 PROTACs (8g, 6, 17b, 14). We therefore treated MV4-11 cells with 8g and 17b, the corresponding ligands 6 and 14, or DMSO and quantified the induced degradation using a label free approach.

2022-01-27 | PXD025257 | Pride

Interaction with WDR5 promotes target gene recognition and tumorigenesis by MYC

Project description:We report a comparison of the genome-wide binding patterns of MYC and WDR5, and the effects of a mutation in MYC (WBM) that disrupt the MYC-WDR5 interaction. The experimental design included two distinct experimental strategies. For comparison of genome-wide binding patters of wild-type (WT) and WDR5 binding-deficient (WBM) MYC, HEK293 cells were engineered by retroviral transduction to express either FLAG-tagged WT-MYC, FLAG-tagged WBM-MYC, or an empty vector control ("vec") ChIP was performed on all samples using the anti-FLAG antibody, and co-precipitating DNAs subject to next-generation sequencing. Samples "2514-WPT-1_1", "2514-WPT-5_1" and "2514-WPT-13_1" are three independent biological replicates of ChIPs performed on the "vec" control cells (i.e., those not expressing any exogenous MYC). Samples "2514-WPT-2_1", "2514-WPT-6_1" and "2514-WPT-10_1" are three independent biological replicates of ChIPs performed on the WT-MYC expressing cells. "2514-WPT-3_1", "2514-WPT-7_1" and "2514-WPT-11_1" are three independent biological replicates of ChIPs performed on the WBM-MYC expressing cells. For comparison of these binding patterns with those of WDR5, we performed ChIP in HEK293 cells with either an antibody against WDR5, or with IgG (negative control). Samples "2514-WPT-23_1", "2514-WPT-25_1", and "2514-WPT-27_1" are independent biological replicates of ChIPs performed with the anti-WDR5 antibody. Samples "2514-WPT-24_1", "2514-WPT-26_1", and "2514-WPT-28_1" are independent biological replicates of ChIPs performed with the negative IgG control.

2015-03-30 | E-GEOD-60897 | biostudies-arrayexpress

Interaction with WDR5 promotes target gene recognition and tumorigenesis by MYC

Project description:We report a comparison of the genome-wide binding patterns of MYC and WDR5, and the effects of a mutation in MYC (WBM) that disrupt the MYC-WDR5 interaction.

2015-03-30 | GSE60897 | GEO

Altered expression of genes in WDR5 knockdown

Project description:WDR5 (WD repeat domain 5) plays an important role in the epigenetic regulation of gene transcription, involing in regulation of embryonic stem cell and cancer cell.Bladder cancer is one of the most common cancers that cause approximately 150,000 deaths per year worldwide.The goal of this study is to identify the target genes of WDR5 in bladder cancer.Our results inditcate that the genes regulated by WDR5 involved in a variety of biological functions, such as proliferation and anti-apoptosis. Bladder cancer cell line UM-UC-3 was transfected with the contol siRNA or two different WDR5 siRNA for 48h. The RNA of the transfected cells was extracted and hybridized on Affymetrix microarrays. We indentified the putative target genes of WDR5 in both WDR5 siRNA by comparing the diferent expressed genes among control, si-WDR5-2 and si-WDR5-3. We futher validated the data of microarray in UM-UC-3 and T24 by RT-qPCR and Western bloting.

2015-02-09 | E-GEOD-59132 | biostudies-arrayexpress

WDR5 high expression and its effect on tumorigenesis in leukemia

Project description:WD repeat domain 5 (WDR5) plays an important role in various biological functions through the epigenetic regulation of gene transcription. However, the oncogenic effect of WDR5 in leukemia remains largely unknown. Here, we found WDR5 expression is increased in leukemia patients. High expression of WDR5 is associated with high risk leukemia; Patients with WDR5 and MLL1 high expression have poor complete remission rate. We further identified the global genomic binding of WDR5 in leukemic cells and found the genomic co-localization of WDR5 binding with H3K4me3 enrichment. Moreover, WDR5 knockdown by shRNA suppresses cell proliferation, induces apoptosis, inhibits the expression of WDR5 targets, and blocks the H3K4me3 enrichment on the promoter of its targets. We also observed the positive correlation of WDR5 expression with these targets in the cohort study of leukemia patients. Our data reveal that WDR5 may have oncogenic effect and WDR5-mediated H3K4 methylation plays an important role in leukemogenesis.

2016-12-30 | GSE72864 | GEO

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